Abstract：
BACKGROUND: Pulmonary fibrosis is a pathological hallmark of lung injury. It is an aggressive disease that replaces normal lung parenchyma by fibrotic tissue. The transforming growth factor-beta-mothers against decapentaplegic homolog 3 (TGF-β1-Smad3) signaling pathway plays a key role in regulating lung fibrosis. Decorin (DCN), a small leucine-rich proteoglycan, has a modulatory effect on the immune system by reversibly binding with TGF-β and reducing its bioavailability. Mesenchymal stem cell (MSC) therapy is a new strategy that has an immune-modulatory capacity.
OBJECTIVE: The aim of this study was to introduce a new therapeutic approach to harness remodeling in injured lung.
METHODS: Bone marrow MSCs were isolated and transduced by decorin gene. Lung injury was induced by bleomycin and mice were treated with MSCs, MSCs-decorin, and decorin. Then, oxidative stress biomarkers, remodeling biomarkers, bronchoalveolar lavage cells, and histopathology study were conducted.
RESULTS: Reduced catalase and superoxide dismutase increased due to treatments. Elevated malondialdehyde, hydroxyproline, TGF-β levels, and polymorphonuclear cells count decreased in the treated groups. Additionally, the histopathology of lung tissues showed controlled inflammation and fibrosis.
CONCLUSIONS: Transfected decorin gene to MSCs and used cell therapy could control remodeling and bleomycin-induced lung injury.
OBJECTIVE: The aim of this study was to introduce a new therapeutic approach to harness remodeling in injured lung.
METHODS: Bone marrow MSCs were isolated and transduced by decorin gene. Lung injury was induced by bleomycin and mice were treated with MSCs, MSCs-decorin, and decorin. Then, oxidative stress biomarkers, remodeling biomarkers, bronchoalveolar lavage cells, and histopathology study were conducted.
RESULTS: Reduced catalase and superoxide dismutase increased due to treatments. Elevated malondialdehyde, hydroxyproline, TGF-β levels, and polymorphonuclear cells count decreased in the treated groups. Additionally, the histopathology of lung tissues showed controlled inflammation and fibrosis.
CONCLUSIONS: Transfected decorin gene to MSCs and used cell therapy could control remodeling and bleomycin-induced lung injury.
摘要：
背景：肺纤维化是肺损伤的病理标志。它是一种侵袭性疾病，由纤维化组织取代正常的肺实质。转化生长因子-β-母亲对抗十指截瘫同系物3（TGF-β1-Smad3）信号通路在调节肺纤维化中起关键作用。Decorin(DCN),一种富含亮氨酸的蛋白多糖，通过与TGF-β可逆结合并降低其生物利用度对免疫系统具有调节作用。间充质干细胞（MSC）治疗是一种具有免疫调节能力的新策略。
目的：本研究的目的是引入一种新的治疗方法来治疗受损肺的线束重塑。
方法：分离骨髓间充质干细胞，并通过核心蛋白聚糖基因转导。博来霉素诱导小鼠肺损伤,MSCs,MSCs-decorin,和装饰。然后，氧化应激生物标志物，重塑生物标志物，支气管肺泡灌洗细胞，并进行组织病理学研究。
结果：由于治疗，过氧化氢酶减少和超氧化物歧化酶增加。丙二醛升高,羟脯氨酸,TGF-β水平,和多形核细胞计数在治疗组减少。此外,肺组织的组织病理学表现为受控的炎症和纤维化。
结论：将核心蛋白聚糖基因转染至骨髓间充质干细胞并使用细胞治疗可以控制重塑和博莱霉素诱导的肺损伤。
目的：本研究的目的是引入一种新的治疗方法来治疗受损肺的线束重塑。
方法：分离骨髓间充质干细胞，并通过核心蛋白聚糖基因转导。博来霉素诱导小鼠肺损伤,MSCs,MSCs-decorin,和装饰。然后，氧化应激生物标志物，重塑生物标志物，支气管肺泡灌洗细胞，并进行组织病理学研究。
结果：由于治疗，过氧化氢酶减少和超氧化物歧化酶增加。丙二醛升高,羟脯氨酸,TGF-β水平,和多形核细胞计数在治疗组减少。此外,肺组织的组织病理学表现为受控的炎症和纤维化。
结论：将核心蛋白聚糖基因转染至骨髓间充质干细胞并使用细胞治疗可以控制重塑和博莱霉素诱导的肺损伤。
